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Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells

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Published on: October 11, 2012

Hemoglobins, programmed cell death and somatic embryogenesis.

Robert D Hill¹, Shuanglong Huang, Claudio Stasolla

¹Department of Plant Science, University of Manitoba, Winnipeg, MB, Canada. rob_hill@umanitoba.ca

Plant Science : an International Journal of Experimental Plant Biology

|August 31, 2013

Summary

Programmed cell death (PCD) involves nitric oxide (NO). Plant hemoglobins can regulate PCD by scavenging NO, influencing plant development and somatic embryogenesis.

Keywords:

2,4-D 2,4-dichlorophenoxyacetic acid ABA Auxin Hb Hemoglobin IAA Nitric oxide PCD PEM Programmed cell death Somatic embryogenesis abscisic acid hemoglobin indoleacetic acid proembryogenic masses programmed cell death

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Area of Science:

Plant biology
Molecular biology
Developmental biology

Background:

Programmed cell death (PCD) is essential for multicellular organism development and stress response.
Nitric oxide (NO) is a key signaling molecule regulating PCD in both plants and animals.
Plant hemoglobins are known to interact with NO, suggesting a role in modulating PCD.

Purpose of the Study:

To review the role of NO and plant hemoglobins in PCD.
To explore how plant hemoglobins influence PCD and somatic embryogenesis.
To understand the mechanism by which NO levels affect embryogenic competence.

Main Methods:

Review of existing literature on PCD, NO, and plant hemoglobins.
Analysis of the role of NO in triggering cell death pathways.
Examination of plant hemoglobin's NO-scavenging activity.
Use of somatic embryogenesis as a model system to study hemoglobin's effect on development.

Main Results:

NO acts as an effector of cell death in plants, initiating cascades leading to targeted cell death.
Plant hemoglobins can interrupt PCD by scavenging NO, thereby promoting cell survival.
Cell-specific expression of plant hemoglobins in somatic embryogenesis affects hormone synthesis, metabolite levels, and PCD-related gene expression.
Altered NO levels impact Zn(2+), reactive oxygen species, and the expression of transcription factor MYC2, influencing embryogenic competence.

Conclusions:

Plant hemoglobins, through cell-specific expression, significantly influence somatic embryogenesis and PCD by modulating cellular NO levels.
The interplay between NO, hemoglobins, and developmental pathways is crucial for regulating plant growth and survival.
Targeting NO levels via hemoglobin activity offers a potential strategy to control plant development and enhance embryogenic competence.